Virologica Sinica

, Volume 26, Issue 2, pp 131–138

Novel evidence suggests Hepatitis B virus surface proteins participate in regulation of HBV genome replication

Authors

  • Jian Qiu
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
    • Graduate University of the Chinese Academy of Sciences
  • Bo Qin
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
    • Graduate University of the Chinese Academy of Sciences
  • Simon Rayner
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
  • Chun-chen Wu
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
  • Rong-juan Pei
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
  • Song Xu
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
  • Xin-wen Chen
    • State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of Sciences
Article

DOI: 10.1007/s12250-011-3190-0

Cite this article as:
Qiu, J., Qin, B., Rayner, S. et al. Virol. Sin. (2011) 26: 131. doi:10.1007/s12250-011-3190-0

Abstract

Naturally occurring mutations in surface proteins of Hepatitis B virus (HBV) usually result in altered hepatitis B surface antigen (HBsAg) secretion efficiency. In the present study, we reported two conserved residues, M75 and M103 with respect to HBsAg, mutations of which not only attenuated HBsAg secretion (M75 only), but also suppressed HBV genome replication without compromising the overlapping p-gene product. We also found M75 and M103 can initiate truncated surface protein (TSPs) synthesis upon over-expression of full-length surface proteins, which may possibly contribute to HBV genome replication. However, attempts to rescue replication-defective HBV mutant by co-expression of TSPs initiated from M75 or M103 were unsuccessful, which indicated surface proteins rather than the putative TSPs were involved in regulation of HBV genome replication.

Key words

Hepatitis B virus (HBV)HBsAgTruncated surface protein (TSPs)Site-directed mutagenesisAlternative translation initiation

Copyright information

© Wuhan Institute of Virology, CAS and Springer-Verlag Berlin Heidelberg 2011